Use of neurophysiological techniques to examine the factors underlying muscle weakness and fatigue after human spinal cord injury (SCI) can provide the vital information needed to develop rational therapeutic strategies for these muscles. Improved muscle function would lead to a more independent lifestyle for that person and provide psychological, economic and societal benefits. The overall objective of this project is to examine mechanisms of force production and fatigue during voluntary contractions of triceps brachii. Data obtained from people with chronic and incomplete cervical SCI (termed SCIin) will be compared to that obtained from able-bodied (control) subjects. Triceps brachii provides an ideal muscle for study since many people with cervical SCI recover limited triceps function, a muscle that is crucial for reaching movements, pushing a wheelchair and weight transfer. Subjects are asked to voluntarily activate triceps brachii at various intensities. We will electrically stimulate the brachial plexus and/or radial nerve to artificially activate the triceps muscle. This approach will yield information about peripheral conduction of triceps motor axons, the electrical and mechanical correlates of the twitch and, when combined with voluntary contractions, the extent of central drive to this motoneuron pool. Central drive and conduction latency will be explored further by using non-invasive magnetic stimulation of the motor cortex. Comparisons between the voluntary and evoked forces will indicate the fraction of muscle under voluntary control. In many cases motor unit firing patterns (rate, variability) will be recorded with selective needle electrodes, also useful for assessing muscle denervation. Modulation of unit firing pattern by cortical stimulation will indicate the influence of motor cortex on single motoneurons. Furthermore, this approach will allow us to examine: 1) the CNS mechanisms governing force production (recruitment, rate-coding) and fatigue; and 2) the mechanical twitch associated with contraction of the motor units. The data obtained will characterize the functional status of triceps brachii in SCIin subjects for the first time. Thus, the neuromuscular consequences of SCIin will be defined at or just below the level of injury, phenomena largely unexplored. Evidence will be sought to show that muscle weakness is primarily due to partial muscle paralysis, that motoneuron loss can occur by direct damage, as well as trans-synaptic degeneration, and that the neuromuscular adaptation which occurs in different subjects reflects the nature of the injury. These subsets of SCIin individuals may best respond to different rehabilitation therapies. Moreover, the sparse interference pattern in most of the muscles after SCIin provides a unique opportunity to follow the behavior of both low and high threshold motor units during repeated submaximal or maximal voluntary contractions. Careful comparisons of these data after specific neurological injury with data from control subjects can add fundamental new information about the interplay between recruitment and rate coding as mechanisms for motor control. Furthermore, the database produced will provide a well understood model of SCIin from which to test the effectiveness of potential rehabilitation strategies.